Transient Receptor Potential (TRP) channels are non-selective cation channels activated by various stimuli such as temperature, chemical compounds, etc., and divided into TRPM, TRPA, TRPV, TRPC, TRPP, TRPML, and TRPN families. Further, the TRPM family includes TRPM1, TRPM2, TRPM3, TRPM4a, TRPM4b, TRPM5, TRPM6, TRPM7 and TRPM8 channels (See, for example, Non-patent literature 1).
TRPM8, also known as CMR1 (cold and menthol sensitive receptor-1), is the eighth member of the TRPM family cloned in 2002 (See, for example, Non-patent literature 2), and is activated by cold temperature (8° C.-28° C.) or chemical compounds which evoke cold sensation such as menthol or icilin (See, for example, Non-patent literature 1 and 2). In addition to the primary afferent nerve (A-delta and C-fibers) and the trigeminal nerve, TRPM8 expression is also reported in taste papillae, vascular endothelium, the aorta, pulmonary arteries, the prostate, the male genital tract (See, for example, Non-patent literature 3), nerve fibers scattered in the human suburothelium (See, for example, Non-patent literature 4), prostate cancer (See, for example, Non-patent literature 5) and oral squamous carcinoma (See, for example, Non-patent literature 6).
In TRPM8 knockout mice, both lack of cold perception and deficiency in hypersensitivity to cold stimulation after nerve injury or inflammation are observed (See, for example, Non-patent literature 3).
In nervous system disorders, increase of TRPM8 expression and involvement in the hypersensitivity to cold in rats with sciatic nerve injury was reported (See, for example, Non-patent literature 7). It is reported that peripheral nerve injury evoked by oxaliplatin increases TRPM8 expression in mice and rats, and that TRPM8 is involved in the cold hypersensitivity evoked by oxaliplatin (See, for example, Non-patent literature 8 and 9). From the fact that patients taking oxaliplatin have increased reactivity to menthol compared with healthy volunteers, TRPM8 is considered to be involved in peripheral neuropathic pain evoked by oxaliplatin in humans as well as in rodents (See, for example, Non-patent literature 10).
In regards to the urinary tract diseases, TRPM8 is reported to be involved in the frequent urination symptoms evoked by cold temperature in rats (See, for example, Non-patent literature 11). Because of the expression in neurons projecting dichotomizing axons into both the skin and the bladder of rats, TRPM8 is considered to be involved in the urinary urgency evoked by cold (See, for example, Non-patent literature 12). In cats and patients with upper central nervous disorders such as stroke and spinal cord injury, infusion of a small amount of cold water into the bladder evokes micturition reflex that is not observed in normal volunteers, and this reflex is increased by the addition of menthol (See, for example, Non-patent literature 13 and 14). In cats, this reflex is decreased according to desensitization of C-fibers, so menthol-sensitive C-fibers are considered to be involved in the reflex (See, for example, Non-patent literature 13).
In patients with idiopathic detrusor overactivity or painful bladder syndrome, it is reported that TRPM8 expression is increased in nerve fibers in the suburothelium, and that TRPM8 expression correlates with the frequency of urination and pain scores (See, for example, Non-patent literature 15). Therefore, it is likely that TRPM8 plays an important role in the bladder afferent pathway during the bladder filling.
Accordingly, treatment or prevention of diseases or symptoms caused by the activation of TRPM8 are expected by inhibiting TRPM8.
In the meantime, as a compound of inhibiting TRPM8, N-(3-aminopropyl)-2-{[(3-methylphenyl)methyl]oxy}-N-(2-thienylmethyl)benzamide hydrochloride (hereinafter sometimes referred to as AMTB) is known.

In anesthetized rats, AMTB suppresses the frequency of rhythmic bladder contractions and nociceptive reflex responses to bladder distension. However, after a high dose of AMTB administration, the decrease of the average blood pressure is observed, so there are still problems (See, for example, Non-patent literature 16).
AMTB has been also disclosed as Examples of a compound represented by the general formula (A) (see Patent literature 1, Example 24).

[wherein, R1, R2, R3, R4, R5, R6, R7 and A have the same meanings as defined in Patent literature 1.]
However, general formula (A) has a different structure from the compounds of the present invention. Further, anything is neither described nor suggested about the compounds of the present invention in Patent literature 1.
In the meantime, a compound represented by the general formula (B) has been described as a α-substituted glycinamide derivative (see Patent literature 2).

[wherein, R1, R2, R3, R5, n, y and z have the same meanings as defined in Patent literature 2.]
However, the compounds described in Patent literature 2 have a different structure from the compounds of the present invention. Further, the compounds of the present invention are different in the point that they are TRPM8 inhibitors relative to that the compound described in Patent literature 2 are oxytocin inhibitors.